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equine endocrine
endrocrine
| Question | Answer |
|---|---|
| EQUINE CUSHING’S DISEASE | known as PARS PITUITARY INTERMEDIA DYSFUNCTION |
| Pars Pituitary intermedia dysfunction Clinical syndrome associated with | hirsutism, polydipsia, polyruia, and hyperglycemia |
| All breeds and types of horses affected | pars pituitary intermedia dysfunction |
| Cushings is a disease | of middle-aged / older horses (> 15 years of age) |
| The diffuse physical enlargement of the pars intermedia results from decreased | dopaminergic innervation from the hypothalamus |
| It is the loss of dopaminergic inhibition which leads to clinical signs of disease | cushings |
| Without dopaminergic inhibition | melanotrope hormone release is increased |
| Without dopaminergic inhibition melanotrope hormone release is increased This is evidenced by | increased and uncontrolled secretion of endorphin (END),melanotropin (MSH), and adrenocorticotropin hormone (ACTH) from proopiomelanocortin peptides in afflicted animals |
| Secondary adrenocortical involvement results from | the secretion of these pituitary hormones |
| Sequela of the | excess circulating glucocorticoids, physical destruction of the pars nervosa, and, likely the direct peripheral action of the pituitary proopiomelanocortin (POMC)-derived peptides |
| Average age of affected horses is | 19 years |
| No sex predilection | equine cushings |
| Hirsutism | long, thick, curly coat that fails to shed |
| It is the most common clinical sign observed | hirsutism |
| Change in shedding behavior and the appearance of guard hairs beneath the mandible, along the chin or distal limbs in the summer may be an early indication of | PPID and may be recognized by owners prior to full-body coat hirsuitism |
| Chronic or recurrent acute laminitis is common and may be the only presenting complaint | PPID |
| Leading cause of euthanasia in horses with | PPID |
| Polyuria and polydipsia are common | PPID |
| Destruction of the pars nervosa by the enlarged pars intermedia leads to | decreased secretion of arginine vasopressin (AVP), originally known as antidiuretic hormone (ADH) |
| Hyperglycemia also promotes | osmotic diuresis |
| Hyperhidrosis | is observed in many horses with PPID |
| Equine sweat glands are under | adrenergic control |
| Neutrophilia with concurrent lymphopenia is | commonly observed |
| Hyperglycemia and insulin-resistance is | present in many cases |
| Definitive diagnostic tests include | Low-dose dexamethasone suppression test Overnight protocol |
| Draw pre-dexamethasone blood sample at | 5 pm, then administer dexamethasone |
| Draw post-dex blood sample | 19 hours later |
| Normal horses | should have good cortisol suppression (<1g/dl) 19 hours after administration of dexamethasone |
| Overnight test is | excellent for screening |
| Seasonal variation – August / September months | may reveal abnormal results (false positive) |
| Most striking necropsy lesion is | pituitary enlargement; attributable to diffuse, adenomatous hyperplasia of the pars intermedia |
| Treatment requires | fastidious management protocols |
| Excellent husbandry and feeding practices and careful management of secondary complications, such as | chronic infections and laminitis |
| The use of a dopaminergic agonist has been associated with | modest declines in POMC peptides as well as improvement in clinical signs |
| Pergolide is a | long-acting dopaminergic agonist |
| Pergolide Side effects | (diarrhea, colic, anorexia) are dose dependent |
| Cyproheptidine is | a drug with anti-serotonergic activity and has been used with limited success |
| Prognosis:Affected horses that are euglycemic | have an excellent long-term prognosis with appropriate management |
| Horses that are mildly hyperglycemic | also generally have a good prognosis but can be more susceptible than euglycemic animals to intercurrent infectious problems |
| Horses that are moderately to severely hyperglycemic (>275 mg/dl) | have a guarded prognosis |
| EQUINE METABOLIC SYNDROME | Similar to human metabolic syndrome in that horses have regional adiposity (deposition of fat along the crest of the neck, tail head, withers) and insulin resistance |
| However, equine metabolic syndrome is | unique |
| Other features of human metabolic syndrome have not been found with EMS such as | hypertension, abdominal adiposity, and microalbuminemia |
| Horses present with obesity (excessive fat accumulation in the body) and a body condition score > 7 / 9 (Henneke scale 1-9), as well as insulin resistance and subclinical / clinical laminitis | equine metabolic syndrome |
| Genetics appear to be associated with the development of | insulin resistance and obesity |
| Ponies tend to be more insulin resistant than horses, although some horse breeds are more prone | Morgans > Arabs > Fjords |
| These horses are typically known as Easy-keepers | in that very little feed keeps horses in heavy body condition |
| Environmental factors also play a role, diet and exercise | equine metabolic syndrome |
| EMS is a disease of adult horses | (> 5 years) with no sex predilection |
| Diagnosis of EMS may be made by | documenting resting hyperinsulinemia |
| Insulin > 20U/mL suggests | insulin resistance |
| Insulin > 30 U/mL defines | hyperinsulinemia |
| Diagnosis may also be confirmed using a combined | glucose-insulin test |
| Field test to detect insulin resistance,collect baseline blood glucose,dminister 150 mg/kg 50pct dextrose IV,Follow with 0 | |
| 10 U/kg insulin IV,Documentation of elevated blood glucose above baseline | for >45 minutes is indicative of insulin resistance |
| EMS management requires | diet and exercise,Weight loss is critical, Remove CHO from diet |
| In EMS Monitor non-structural CHO in hay | Should be < 12pct,Soaking hay prior to feeding decreaes CHO |
| Feed grass hay for EMS | 1 |
| 5 – 2 | |
| 0pct of body weight / day based on goal weight | |
| Restrict pasture grazing and | encourage use of grazing muzzle |
| Exercise is important in EMS but | may be difficult with clinical laminitis |
| Once the EMS condition is stabilized | hand-walking is encouraged |
| Swimming is ideal for EMS | |
| Additional therapy: Levothyroxine for EMS | May lower body weight / improve insulin sensitivity |
| Prescribe until reach ideal body weight | Levothyroxine |
| Do not use for >6 months | Levothyroxine |
| Equine hypothyroidism | is poorly understood and many theories / etiologies have yet to be substantiated (ie laminitis,obesity,rhabdomyolysis,anhidrosis) |
| Hypothyroidism should be considered in the differential of any horse presenting with a history of | lethargy, poor exercise tolerance, or muscular problems |
| It may be difficult to confirm the diagnosis due to challenges of performing testing in the field | hypothyroidism |
| The diagnosis of hypothyroidism is most commonly based on | low serum concentrations of total T4 and T3, but may be more definitively diagnosed following TSH / TRH stimulation tests |
| Although some will suggest response to thyroid supplementation is diagnostic | the placebo affect may conflict interpretation |
| Endophyte alkaloids (produced by a symbiotic fungus living on the fescue grass) | act as dopamine agonists |
| TSH is | inhibited by dopamine – as a result, it has been suggested that fescue consumption can lead to hypothyroidism |
| May see prolonged gestation and agalactia | fescue hypothyroidism |
| Treatment fescue hypothyroidism | domperidone (dopamine antagonist) |
| At birth, the normal foal has plasma concentrations of thyroxine (T4) and triiodothyronine (T3) | 10-20 times greater than the adult and also greater than reported in any other species |
| Hyperplastic goiter in neonates | is the most common thyroid disorder in the horse |
| It is thought to result from the mare’s excess iodine consumption or plant goitrogens during gestation | hyperplastic goiter in neonates |
| An additional syndrome of dysmaturity (prolonged gestation), mandibular pragnathism and incomplete ossification has also been reported | in foals of the western USA and Canada |
| Caution is warranted with thyroid supplementation | without confirmation of diagnosis, as the associated health risks in horses is largely unexplored |
| In humans, health risks include | decreased bone density and increased risk of atrial fibrillation, myocardial infarction, and congestive heart failure |
| Thyroid adenomas | relatively common and may be easily palpable as enlarged gland in the cranial neck alongside the proximal trachea in the adult horse |
| Most thyroid tumors | are benign and nonfunctional and thyroid hormones remain WNL |
| Treatment is unnecessary unless the mass becomes large enough to compress the respiratory and/or ailmentary tracts | thyroid adenoma |
| If thyroidectomy is required, appropriate | thyroid hormone supplementation is warranted |
| Diabetes insipidus | results from decreased release of ADH from the posterior pituitary |
| The most common cause of decreased ADH release in the horse is | posterior pituitary destruction secondary to pars intermedia enlargement, but rare cases of primary diabetes insipidus have been reported |
| Diabetes insipidus Clinical presentation | PU/PD in an otherwise normal animal, azotemia is NOT present |
| Diabetes insipidus | Urine specific gravity < 1 |
| 010 and the patient fails to concentrate urine on a water deprivation test | |
| Psychogenic polydypsia syndrome is | observed as a stable vice in some horses |
| These patients are able to concentrate urine (> 1 | |
| 025) when they are subjected to water deprivation test | pshychogenic polydypsia |
| Nutritional hyperparathyroidism (Big head / Bran disease / Miller’s disease) | was formerly the most common cause of hyperparathyroidism in the horse |
| This condition has become rare as knowledge of proper equine nutrition has become more widespread | nutritional hyperparathyroidism |
| A relative calcium deficiency secondary to excess dietary phosphorus lead to the clinical signs of | Big Head disease |
| Clinical signs include facial bone enlargement, difficulty in mastication due to bone loss, fractures of the molars, spontaneous long bone fractures may occur, unthriftiness, shifting lameness and physitis / limb deformities in young animals | Big Head disease |
| Upper airway noise may be heard due to narrowing of the nasal passages with | bony remodeling |
| Elevated phosphorus and decreased calcium | lead to hyperplasia of the parathyroid gland |
| PTH | secretion inhibits Vitamin D synthesis, increases bone resorption and bone loss (primarily of bones in the face) |
| The bone loss is replaced | by un-mineralized connective tissue |
| Most patients remain | normocalcemic as this disease is very slowly progressive, calcium levels are maintained |
| Radiographs are helpful only if | >30pct of mineral loss has occurred |
| Treatment involves | elimination of grain in the diet as well as feeds that contain excess oxalates |
| Supplementation of calcium is warranted, typically | in the form of calcium carbonate (limestone) |
| The ideal ratio is Ca:P between 3:1 and 4:1 | for supplementation therapy |
| Recovery is possible, but | requires many months and some bony abnormalities may not be resolved |
| Vitamin D toxicosis | can result from overzealous administration of vitamin D containing nutritional supplements or ingestion of plants with leaves that have vitamin D like biologic activity |
| Example = Cestrum diurnum | plants with leaves that have vitamin D like biologic activity |
| These horses have elevated serum calcium with normal serum phosphorus | vitamin D toxicosis |
| Vitamin D toxicosis | Pathologic calcification of soft tissue is widespread in arteries, tendons, and ligaments |
| Prognosis is poor | Vitamin D toxicosis once pathologic calcification of soft tissue is present |
Created by:
alljacks
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